DDAH1 Human

DDAH1 is part of the DDAH family of enzymes, which also includes DDAH2. These enzymes are responsible for the breakdown of ADMA and monomethyl arginine (L-NMMA), both of which inhibit NOS activity. By metabolizing these inhibitors, DDAH1 helps regulate the levels of NO, a critical signaling molecule involved in various physiological processes such as vascular tone regulation, inflammation, and angiogenesis .

ADMA is considered an independent risk factor for cardiovascular diseases. Elevated levels of ADMA can lead to reduced NO production, resulting in endothelial dysfunction and increased risk of atherosclerosis, hypertension, and other cardiovascular conditions. DDAH1, by metabolizing ADMA, helps maintain NO levels and thus protects against these cardiovascular risks .

Research has shown that manipulating the DDAH/ADMA/NO pathway can have significant therapeutic benefits. For instance, increasing DDAH1 activity or expression could potentially lower ADMA levels, thereby enhancing NO production and improving cardiovascular health. Conversely, inhibiting DDAH1 activity has been explored as a strategy to reduce NO levels in certain pathological conditions, such as cancer, where NO can promote tumor growth and angiogenesis .

Human recombinant DDAH1 is produced using recombinant DNA technology, which involves inserting the gene encoding DDAH1 into a suitable expression system, such as bacteria or yeast, to produce the enzyme in large quantities. This recombinant enzyme is used in various research and therapeutic applications to study its function and potential as a therapeutic target .